More bone with less minerals? The effects of dietary phosphorus on the post-cranial skeleton in zebrafish

Dietary phosphorus (P) is essential for bone mineralisation in vertebrates. P deficiency can cause growth retardation, osteomalacia and bone deformities, both in teleosts and in mammals. Conversely, excess P supply can trigger soft tissue calcification and bone hypermineralisation. This study uses a...

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Bibliographic Details
Published in:International Journal of Molecular Sciences
Main Authors: Cotti, Silvia, Huysseune, Ann, Koppe, Wolfgang, Rucklin, Martin, Marone, Federica, Woelfel, Eva M., Fiedler, Imke A. K., Busse, Bjoern, Forlino, Antonella, Witten, Paul Eckhard
Format: Article in Journal/Newspaper
Language:English
Published: 2020
Subjects:
Biology and Life Sciences
mineralisation
bone formation
vertebral column
vertebral body fusion
collagen
SALMON SALMO-SALAR
JUVENILE ATLANTIC SALMON
TELEOST FISH
VERTEBRAL ABNORMALITIES
COMPARATIVE VIEW
AXIAL SKELETON
DANIO-RERIO
X-RAY
MINERALIZATION
PHOSPHATE
Atlantic salmon
Salmo salar
Online Access:https://biblio.ugent.be/publication/8737469
http://hdl.handle.net/1854/LU-8737469
https://doi.org/10.3390/ijms21155429
https://biblio.ugent.be/publication/8737469/file/8763402
Description
Summary:Dietary phosphorus (P) is essential for bone mineralisation in vertebrates. P deficiency can cause growth retardation, osteomalacia and bone deformities, both in teleosts and in mammals. Conversely, excess P supply can trigger soft tissue calcification and bone hypermineralisation. This study uses a wide range of complementary techniques (X-rays, histology, TEM, synchrotron X-ray tomographic microscopy, nanoindentation) to describe in detail the effects of dietary P on the zebrafish skeleton, after two months of administering three different diets: 0.5% (low P, LP), 1.0% (regular P, RP), and 1.5% (high P, HP) total P content. LP zebrafish display growth retardation and hypomineralised bones, albeit without deformities. LP zebrafish increase production of non-mineralised bone matrix, and osteoblasts have enlarged endoplasmic reticulum cisternae, indicative for increased collagen synthesis. The HP diet promotes growth, high mineralisation, and stiffness but causes vertebral centra fusions. Structure and arrangement of bone matrix collagen fibres are not influenced by dietary P in all three groups. In conclusion, low dietary P content stimulates the formation of non-mineralised bone without inducing malformations. This indicates that bone formation and mineralisation are uncoupled. In contrast, high dietary P content promotes mineralisation and vertebral body fusions. This new zebrafish model is a useful tool to understand the mechanisms underlying osteomalacia and abnormal mineralisation, due to underlying variations in dietary P levels.

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